ULK1 Double Nickase Plasmid (m): sc-423606-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ULK1 Double Nickase Plasmid (m) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- ULK1 Double Nickase Plasmid (m) and ULK1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ulk1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ULK1 Antibody (F-4): sc-390904
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ULK1 Double Nickase Plasmid (m) | sc-423606-NIC | 20 µg | $410.00 | |||
ULK1 Double Nickase Plasmid (m2) | sc-423606-NIC-2 | 20 µg | $410.00 |
Mouse Ulk1 encodes ULK1, a serine/threonine kinase that functions as a core initiator of macroautophagy by integrating nutrient and energy status cues. ULK1 forms an initiation complex with ATG13, FIP200/RB1CC1, and ATG101 and is regulated by AMPK and mTORC1 to control autophagosome biogenesis during starvation and cellular stress. Through phosphorylation of downstream autophagy factors, ULK1 coordinates membrane recruitment and early autophagic signaling that influences proteostasis, mitochondrial quality control, and innate immune responses. Dysregulated ULK1-dependent autophagy has been linked to neurodegeneration, infection biology, metabolic dysfunction, and cancer-associated stress adaptation, making Ulk1 a frequent target in pathway dissection studies.
ULK1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ulk1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ulk1. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt Ulk1 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of Ulk1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.